PRIMARY: caused by an aldosterone-secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma rennin.
Increased aldosterone secretion from adrenal, which results primary from 2 major subtypes:
1) Unilateral aldosterone-producing adenoma (APA) or Conn ’s syndrome, the most common subtype (50-60% of case), usually small <3 cm unilateral, and rennin-unresponsive. This means that aldosterone secretion is not affected by changes en posture. Rarely, the adenoma is rennin-responsive (aldosterone levels increase with standing).
2) Idiopathic hyperaldosteronism (IHA) or bilateral adrenal hyperplasia. Aldosterone increases in response to postural studies. Rarely, patients are hyperplastic (primary adrenal hyperplasia), and the response of aldosterone to standing is similar to rennin-unresponsive APA
Other subtypes:
3) Rennin-responsive adenoma
4) Primary adrenal hyperplasia
5) Glucocorticoids-remediable aldosteronism.
Aldosterone, by inducing renal distal tubular reabsortion of sodium, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, alkalosis.
Hypokalemia → fatigue, muscle weakness, cramping, headaches, and palpitations.
Polydipsia and polyuria from hypokalemia-induced nephrogeni diabetic insipidus.
Treatment: the goal of treatment is to prevent the morbidity and mortality associated with hypertension and hypokalemia. Appropriate treatment depends on the cause e.g. Conn ’s syndrome vs. IHA (unilateral or bilateral adrenalectomy).
Medication: spironolactone (aldosterone antagonists).
SECUNDARY: Due to: Renal artery stenosis
Chronic renal failure
CHF
Cirrhosis
Nephrotic syndrome
Kidney perception of low intravascular volume results in an overactive rennin-angioitensin system. Associated with high plasma rennin.
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